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The Vo2max and the Central Governor: a Different Understanding

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The Vo2max and the Central Governor: a Different Understanding In: Regulation of Fatigue in Exercise ISBN 978-1-61209-334-5 Editor: Frank E. Marino © 2011 Nova Science Publishers, Inc. The exclusive license for this PDF is limited to personal website use only. No part of this digital document may be reproduced, stored in a retrieval system or transmitted commercially in any form or by any means. The publisher has taken reasonable care in the preparation of this digital document, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained herein. This digital document is sold with the clear understanding that the publisher is not engaged in rendering legal, medical or any other professional services. Chapter 5 THE VO2MAX AND THE CENTRAL GOVERNOR: A DIFFERENT UNDERSTANDING Timothy David Noakes UCT/MRC Research Unit for Exercise Science and Sports Medicine, Department of Human Biology, University of Cape Town and Sports Science Institute of South Africa, Boundary Road, Newlands, 7700, South Africa ABSTRACT In 1923, Nobel Laureate A.V. Hill introduced his cardiovascular/ anaerobic/ catastrophic model of human exercise performance. According to this model, maximal exercise testing for the measurement of the maximum oxygen consumption (VO2max) terminates when the maximum rate of oxygen delivery to the exercising muscles is less than their peak rate of oxygen demand. As a result skeletal muscle anaerobiosis develops, causing fatigue and the termination of exercise. The weakness of this interpretation is that it is “brainless” since it excludes any role for the brain in determining maximal exercise performance. Yet without the brain, there can be no skeletal muscle recruitment, without which exercise cannot occur. The analogy is a racing car: A racing car filled with petrol will not move off the starting grid until the brain of the racing driver starts the car‟s engine, engages first gear and applies pressure to the car‟s accelerator. The role of the brain in exercise performance is identical; until the muscles are recruited by the motor cortex, they will not function; without increasing skeletal muscle recruitment, the oxygen consumption and cardiac output cannot rise. Thus it is the level of skeletal muscle recruitment that must determine the athlete‟s maximal work rate as well as the extent to which the cardiac output and oxygen consumption rise during the VO2max test. Remarkably the Hill model has instilled the reverse doctrine specifically that the cardiac output, not the level of skeletal muscle recruitment, determines the work output of the muscles. In this chapter I present 6 biological predictions of the Hill model of maximal exercise performance that have been disproven specifically that (i) the “plateau phenomenon” does not occur in 100% of subjects during VO2max testing; (ii) skeletal muscle anaerobiosis does not occur during maximal exercise; (iii) the cardiac output does 80 Timothy David Noakes not show a “plateau phenomenon” nor (iv) are all available motor units activated in the exercising limbs of all subjects during VO2max testing; (v) fatigue does not always develop at the same level of “fatiguing” metabolites; and (vi) fatigue is never absolute. Instead the evidence is that the VO2max test is a submaximal test that is terminated by the brain when less than 100% of the motor units in the exercising limbs have been recruited. The protected variable that triggers this anticipatory termination of the VO2 max test is currently unknown but may well relate to changes in cerebral oxygenation. INTRODUCTION On the basis of his interpretation that fatigue is caused by anaerobiosis in the exercising muscles as a result of the development of myocardial ischaemia, in 1923 Professor Archibald Vivian Hill introduced the concept of the maximum oxygen consumption (VO2max) into the exercise sciences (Chapter 1). In 1955 H.L. Taylor and colleagues[1] established this concept by stating that: “The classic work of Hill has demonstrated that there is an upper limit to the capacity of the combined respiratory and cardiovascular systems to transport oxygen to the muscles. There is a linear relationship between oxygen intake and work rate until the maximum oxygen intake is reached. Further increases in workload beyond this point merely result in an increase in oxygen debt and a shortening of the time in which the work can be performed”. These scientists were also the first to describe the concept that would become known as the “plateau phenomenon”: “Each day the (running) speed was increased until the oxygen uptake during the standard collection time reached a plateau”. In the past 50 years few have felt it necessary to question the veracity of these concepts. Those who have dared[2-5], have usually attracted a dismissive response[5-15] suggesting that new ideas are not always welcome in the exercise sciences. In a recent publication Mitchell and Saltin[16] provided their most current interpretation of Hill‟s contribution to our understanding of the physiological basis for the VO2max: “It is noteworthy that although well-designed treadmills were available, Hill preferred walking and running in the field or on the track for his experiments. To determine the velocity of the runner, he developed a sophisticated electromagnetic system that provided split times for every 25 yards. In the experiments on Hill himself, a levelling off in VO2 was observed, not as a function of increasing speed of running, but with the time at the highest velocity, which was 260 meters.min-1[17]. Noakes has challenged whether Hill actually demonstrated a plateau in VO2 and thus had measured a true VO2max[3]. Hill appears to have accomplished this in the experiments conducted on himself; but more importantly, he was the one who conceived the physiological meaning of maximal VO2.” Elsewhere [18, 19] I have provided the contradictory evidence which shows that Hill was absolutely convinced that his model of the physiological factors limiting the VO2max was beyond doubt. So why would he have considered it necessary to “prove” this theory by showing the presence of the “plateau phenomenon”? In his mind he had already done that. Only later, when his theory began to be questioned for the first time, did a modern generation of scientists feel the urgent need to “prove” that Hill‟s ideas were correct by attempting to show that the “plateau phenomenon” or some equivalent [10, 11, 15, 20, 21] always causes the termination of exercise in all VO2max tests (as is required by the Hill model). The VO2MAX and the Central Governor 81 In fact, as argued in Chapter 1, the real test of a maximal effort according to the Hill model must be the development of myocardial ischaemia and cardiac failure, according to Hill‟s idea that: “When the oxygen supply becomes inadequate, it is probable that the heart rapidly begins to diminish its output, so avoiding exhaustion”[22]. However the well-established finding that myocardial ischaemia does not occur during maximal exercise in healthy subjects [23] disproves this component of Hill‟s model. Not surprisingly protagonists of this model chose to ignore this inconvenient finding, continuing rather to argue that it is the presence of a “plateau phenomenon”, defined in at least 10 different ways [24] that proves the model. Whereas I argue that according to the Hill model the sole proof that a VO2max test is “truly maximal” is the development of myocardial ischaemia. Or alternatively that exercise terminates only after all the available motor units in the active limbs have been recruited (Chapter 1). Mitchell and Saltin[16] included a diagram, redrawn here as Figure 1, which explained why they believe the VO2max is limited by the maximum cardiac output and the maximum systemic arterio-venous oxygen difference. According to this (Hill) model, three factors, namely cardiovascular function (specifically the maximum cardiac output), the blood haemoglobin concentration, and the extent to which oxygen is extracted from the arterial blood by the active muscles determine the magnitude of the VO2max. The focus of this chapter is to argue that the model depicted in Figure 1 is only valid if exercise is indeed limited by a failure of oxygen delivery to the exercising muscles as Hill had presumed in 1923 but which, I argue, his data did not ever prove [4, 18, 24, 25]. Maximal oxygen uptake Maximal cardiac output Maximal systemic a-VO2 difference Maximal Maximal stroke Maximal arterial O2 Minimal mixed heart rate volume content venous O2 content Maximal Minimal Hemoglobin % O2 Redistribution Extraction end-diastolic end-systolic concentration saturation of blood of O2 volume volume flow Figure 1. The physiological factors that determine or “limit” the maximum oxygen consumption (VO2max) according to the traditional A.V. Hill model. After Mitchell and Saltin [16]. 82 Timothy David Noakes MOTOR UNIT RECRUITMENT Number Frequency 1.RESPIRATION 4.CENTRAL CIRCULATION Maximum ventilation Coronary blood flow Alveolar ventilation: Myocardial contractility perfusion ratio Cardiac output Alveolar – arterial O2 diffusion Pulmonary capillary pressure Haemoglobin – O2 affinity Systemic blood pressure [Haemoglobin] 2.PERIPHERAL CIRCULATION 3.MUSCLE CONTRACTION / METABOLISM Muscle blood flow Muscle mass Muscle vasodilatory capacity Muscle fiber type Muscle capillary density Muscle contractility Capillary O2 diffusion Mitochondria – size and number Mitochondrial O2 extraction [Myoglobin] Haemoglobin-O2 affinity Energy stores Flow to non-exercising regions Substrate delivery Hormonal response Figure 2. The popular diagram showing the four physiological systems (respiration, peripheral circulation, central circulation and muscle contraction/metabolism) that are believed to “limit” the VO2max according to the traditional A.V. Hill model. The missing element in this diagram is the central nervous system. Without the recruitment of sufficient motor units in the limbs, movement and hence exercise is not possible. Without an increased skeletal muscle recruitment, there can be no increase in VO2.
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